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[肾性贫血血液透析患者α2-肾上腺素能受体功能紊乱——与重组人促红细胞生成素相关的血压升高的可能原因?]

[Disordered alpha 2-adrenoreceptor function in hemodialysis patients with renal anemia--a possible cause of increased blood pressure in relation to recombinant human erythropoietin?].

作者信息

Müller R, Steffen H M, Brunner R, Pollok M, Baldamus C A, Kaufmann W

机构信息

Medizinische Klinik II, Universität Köln.

出版信息

Klin Wochenschr. 1991 Oct 18;69(16):742-8. doi: 10.1007/BF01797612.

Abstract

Nine patients on maintenance hemodialysis and transfusion-demanding renal anemia (group A) were treated with rHuEPO 120 IU/kg i.v. three times per week. Hemoglobin-content was raised from 7.2 +/- 0.9 to 10.4 +/- 0.8 g/dl. In all patients blood pressure rose, three patients developed arterial hypertension. Mean diastoloic blood pressure was 66 +/- 12 and 78 +/- 16 mmHg (p less than 0.001) before and after rHuEPO. Rise in blood pressure was accompanied by a significant fall in plasma-noradrenaline-levels (from 498 +/- 100 to 383 +/- 75 pg/ml; p less than 0.05) and alpha 2-adrenoceptor-density (from 574 +/- 76 to 384 +/- 49; p less than 0.05). Compared to nine patients on maintenance hemodialysis and hematocrit over 30% (group B), patients with severe renal anemia (group A before treatment) had higher densities of alpha 2-adrenoceptors (574 +/- 76 vs. 218 +/- 32; p less than 0.001) despite higher plasma-noradrenaline-levels (498 +/- 100 vs. 399 +/- 63; n.s.). We suppose a anemia-related disturbance of alpha 2-receptor-function with the result of abolished receptor down-regulation and impaired vascular reagibility to vasoconstricting stimuli. With the correction of anemia receptor-function improves, receptor down-regulation as well as vascular reagibility is re-established resulting in augmented vascular resistance and higher blood pressure.

摘要

9例维持性血液透析且有输血需求的肾性贫血患者(A组),接受重组人促红细胞生成素(rHuEPO)静脉注射,剂量为120 IU/kg,每周3次。血红蛋白含量从7.2±0.9g/dl升至10.4±0.8g/dl。所有患者血压均升高,3例患者出现动脉高血压。rHuEPO治疗前后平均舒张压分别为66±12mmHg和78±16mmHg(p<0.001)。血压升高伴随血浆去甲肾上腺素水平显著下降(从498±100pg/ml降至383±75pg/ml;p<0.05)以及α2-肾上腺素能受体密度下降(从574±76降至384±49;p<0.05)。与9例维持性血液透析且血细胞比容超过30%的患者(B组)相比,重度肾性贫血患者(治疗前A组)尽管血浆去甲肾上腺素水平较高(498±100 vs. 399±63;无统计学差异),但其α2-肾上腺素能受体密度更高(574±76 vs. 218±32;p<0.001)。我们推测与贫血相关的α2受体功能紊乱导致受体下调缺失以及血管对血管收缩刺激的反应性受损。随着贫血的纠正,受体功能改善,受体下调以及血管反应性得以重建,从而导致血管阻力增加和血压升高。

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